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AIM: To investigate whether acute lung injury (ALl) in ventilated piglets with bacterial infection affects NF-κB and AP-1 expression in alveolar macrophages (AM) and whether nitric oxide (NO), surfactant (Surf), glucocorticoids (GC) affect NF-κB and AP-1 activation in AM in vivo and in vitro. METHODS: The animals were intraperitoneally injected Escherichia coli, which caused ALl. Nuclear extracts of AM were analyzed by electrophoretic mobility shift assay (EMSA) for the nuclear factor-kappa B (NF-κB) and activation protein-1 (AP-1) expression. Detection of IκB-α protein was from cytoplasmic extract by Western blotting. Immunocytochemistry staining was used for intracellular location of p65 subunits of NF-κB. RESULTS: In ex vivo experiments, strikingly higher expression of NF-κB and AP-1 by EMSA was found 6 h after bacterial injection in contrast to the Normal group. In the NO, SNO, and GC groups, markedly attenuated NF-κB and AP-1 activation was observed. The NF-κB and AP-1 activation in Surf g
AIM: To investigate whether acute lung injury (ALl) in ventilated piglets with bacterial infection affects NF-κB and AP-1 expression in alveolar macrophages (AM) and whether nitric oxide (NO), surfactant (Surf), glucocorticoids (GC) affect METHODS: The animals were intraperitoneally injected in Escherichia coli, which caused ALI. Nuclear extracts of AM were analyzed by electrophoretic mobility shift assay (EMSA) for the nuclear factor-kappa Detection of IκB-α protein was from cytoplasmic extract by Western blotting. Immunocytochemistry staining was used for intracellular location of p65 subunits of NF-κB. RESULTS: In: (B-NF-κB) and activation protein-1 ex vivo experiments, strikingly higher expression of NF-κB and AP-1 by EMSA was found after 6 h after bacterial injection in contrast to the normal group. In the NO, SNO, and GC groups, markedly attenuated NF-κB and AP-1 activation was observed. The NF-κB and AP-1 ac tivation in Surf g